Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Anti-infective therapeutics' effect on the microbiome

ABSTRACT: Modifications to the gut microbiome in response to various anti-bacterial therapeutics.

PROVIDER: PRJEB34462 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	ERR3588250_1.fastq.gz	Fastqsanger.gz
	ERR3588250_2.fastq.gz	Fastqsanger.gz
	ERR3588260_1.fastq.gz	Fastqsanger.gz
	ERR3588260_2.fastq.gz	Fastqsanger.gz
	ERR3588270_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 828

Similar Datasets

The combination of cantharidin and anti-angiogenic therapeutics presents synergistic antitumor effects against pancreatic cancer

Project description:The combination of cantharidin and anti-angiogenic therapeutics presents synergistic antitumor effects against pancreatic cancer

| PRJNA459723 | ENA

Bile acid therapeutics for NASH

Project description:Bile acid therapeutics for NASH

| PRJNA705980 | ENA

The combination of cantharidin and anti-angiogenic therapeutics presents synergistic antitumor effects against pancreatic cancer

Project description:Background: Cantharidin, an active constituent of mylabris, is believed to have anti-tumor activity. Cantharidin selectively inhibit protein phosphatase 2A (PP2A), a repressor of oncogenic kinase pathways (ERK, JNK, NF-κB, and PKC). Cantharidin represses the growth and metastasis of pancreatic cancer cells in vitro. In the present study, we investigated the effects of cantharidin on pancreatic cancer xenografts in vivo. Methods: Cells stably expressing luciferase were used to establish xenograft models. Xenograft growth was evaluated by living imaging. Gene expression was determined using a microarray, real-time PCR, a RayBiotech antibody array, and the Milliplex assay. Results: Surprisingly, cantharidin significantly accelerated xenograft growth. Living imaging showed a rapid distribution of D-luciferin in cantharidin-treated xenografts, suggesting a rich blood supply. Immunohistochemistry confirmed increased angiogenesis. Microarray and antibody array identified upregulated pro-angiogenic and downregulated anti-angiogenic factors. The Milliplex assay suggested elevated secretion of IL-6, IL-8, TNF-α, and VEGF. ERK, JNK, NF-κB, and PKC pathway inhibitors attenuated the cantharidin-induced changes to pro-angiogenic gene expression. PKC pathway-inhibiting tamoxifen or antiangiogenic therapeutics, including Ginsenoside Rg3, bevacizumab, Apatinib, and Endostar antagonized the pro-angiogenic effect of cantharidin or its derivatives. These regimens presented remarkable synergistic antitumor effects in vivo. Conclusion: Although cantharidin presents anti-tumor effects in vitro and has been applied in clinical practice, we revealed an unfavorable pro-angiogenic side effect. We recommend that the clinical application of cantharidin should be performed on the premise of anti-vascularization therapy.

2018-12-06 | GSE114040 | GEO

Enantioselective Interactions of Anti-Infective 8-Aminoquinoline Therapeutics with Human Monoamine Oxidases A and B.

Project description:8-Aminoquinolines (8-AQs) are an important class of anti-infective therapeutics. The monoamine oxidases (MAOs) play a key role in metabolism of 8-AQs. A major role for MAO-A in metabolism of primaquine (PQ), the prototypical 8-AQ antimalarial, has been demonstrated. These investigations were further extended to characterize the enantioselective interactions of PQ and NPC1161 (8-[(4-amino-1-methylbutyl) amino]-5-[3, 4-dichlorophenoxy]-6-methoxy-4-methylquinoline) with human MAO-A and -B. NPC1161B, the (R)-(-) enantiomer with outstanding potential for malaria radical cure, treatment of visceral leishmaniasis and pneumocystis pneumonia infections is poised for clinical development. PQ showed moderate inhibition of human MAO-A and -B. Racemic PQ and (R)-(-)-PQ both showed marginally greater (1.2- and 1.6-fold, respectively) inhibition of MAO-A as compared to MAO-B. However, (S)-(+)-PQ showed a reverse selectivity with greater inhibition of MAO-B than MAO-A. Racemic NPC1161 was a strong inhibitor of MAOs with 3.7-fold selectivity against MAO-B compared to MAO-A. The (S)-(+) enantiomer (NPC1161A) was a better inhibitor of MAO-A and -B compared to the (R)-(-) enantiomer (NPC1161B), with more than 10-fold selectivity for inhibition of MAO-B over MAO-A. The enantioselective interaction of NPC1161 and strong binding of NPC1161A with MAO-B was further confirmed by enzyme-inhibitor binding and computational docking analyses. Differential interactions of PQ and NPC1161 enantiomers with human MAOs may contribute to the enantioselective pharmacodynamics and toxicity of anti-infective 8-AQs therapeutics.

| S-EPMC8146505 | biostudies-literature

Deferoxamine as adjunct therapeutics for tuberculosis.

Project description:Deferoxamine as adjunct therapeutics for tuberculosis.

| PRJNA1103242 | ENA

ProCTLA-4 in anti-tumor immunity

Project description:We developed a prodrug of the anti-CTLA4 antibody, named ProCTLA-4. ProCTLA-4 elicits anti-tumor immune responses with reduced toxicity compared to current CTLA4 blockade therapies. Moreover, compared to currently used Probody Therapeutics targeting CTLA-4, ProCTLA-4 offers significant advantages for enhanced efficacy. Thus, our design establishes an alternative paradigm for antibody therapeutics that enables reduction of irAEs while simultaneously increasing therapeutic efficacy.

2025-08-20 | GSE305582 | GEO

Partitioning of cancer therapeutics in nuclear condensates

Project description:Partitioning of cancer therapeutics in nuclear condensates

| PRJNA627353 | ENA

MicroRNA therapeutics for stratified treatment of Schizophrenia

Project description:MicroRNA therapeutics for stratified treatment of Schizophrenia

| PRJNA929968 | ENA

ChIP-seq of resting and anti-CD3/CD28-stimuated Jurkat cells

Project description:To finely dissect the dynamic changes in the epigenome and chromatin state during T cell activation, we utilized the Jurkat cell line as a model and performed ChIP-seq on both resting and anti-CD3/CD28-stimulated Jurkat cells, targeting various histone modifications (H3K27ac, H3K4me1, H3K4me3, H3K27me3), RNA PolII, and CTCF.

2025-09-01 | GSE277460 | GEO

Integrated transcriptomic and in silico drug screening identifies potential stroma-targeting therapeutics in pancreatic cancer

Project description:This study identifies a gene panel that can distinguish two stromal subgroups of resected pancreatic cancers which have different microenvironment features and prognosis, and can be targeted by different therapeutic approaches. In-silico and in-vitro analysis indicates that our proposed signature could be further investigated as a predictor of response of immunomodulatory agents, including anti CD40 therapeutics

2025-02-10 | GSE196524 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data